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However, the splicing landscape of\n                  <jats:italic>NRXN1<\/jats:italic>\n                  across distinct human brain cell types remains poorly defined. Because\n                  <jats:italic>NRXN1<\/jats:italic>\n                  expression level is relatively low in adult brains and human induced pluripotent stem cell (hiPSC) derived neurons, single-cell long-read cDNA sequencing often provides insufficient coverage to capture its full isoform diversity, particularly across heterogeneous cell populations. To address this gap, we developed an integrative sequencing strategy that combines single-cell transcriptomics, targeted enrichment of\n                  <jats:italic>NRXN1<\/jats:italic>\n                  transcripts, and long-read sequencing. This approach reveals a comprehensive catalog of cell-type resolved\n                  <jats:italic>NRXN1<\/jats:italic>\n                  isoforms across adult and fetal human postmortem brains as well as hiPSC-derived cortical organoids. From the adult prefrontal cortex (PFC) region, our analyses reveal distinct splicing programs across interneuron subtypes, pyramidal neurons, and glial lineages. Comparisons between prenatal and adult brains indicate that\n                  <jats:italic>NRXN1<\/jats:italic>\n                  isoform profiles are established during early development and remain stable throughout neuronal maturation. In hiPSC organoid models, splicing profiles partially mirror both developmental and mature brain patterns, with a subset of splice sites exhibiting cell type \u2013 and stage-specific divergence. In the cerebellum of an autism case and in organoids derived from schizophrenia patients, carrying non-recurrent heterozygous\n                  <jats:italic>NRXN1<\/jats:italic>\n                  deletions, we identify disrupted isoform expression and mutant\n                  <jats:italic>NRXN1\u03b1<\/jats:italic>\n                  isoforms and characterize their distribution across diverse cell types. Using this integrated long-read sequencing framework in patient-derived organoids, we further show that antisense oligonucleotide (ASO) targeting of mutant splice junctions reduces gain-of-function\n                  <jats:italic>NRXN1<\/jats:italic>\n                  isoforms and reshapes splicing patterns in a cell type\u2013specific manner, providing a platform for evaluating ASO efficiency. Together, these findings help understand the cell type\u2013specific splicing landscape of\n                  <jats:italic>NRXN1<\/jats:italic>\n                  and establish a framework for decoding cell type-specific isoform diversity and assessing transcript-targeted therapies for genes with low expression levels.\n                <\/jats:p>","DOI":"10.1101\/2025.11.11.687875","type":"posted-content","created":{"date-parts":[[2025,11,12]],"date-time":"2025-11-12T09:20:12Z","timestamp":1762939212000},"source":"Crossref","is-referenced-by-count":1,"title":["Cell-type-resolved\n                  <i>NRXN1<\/i>\n                  isoforms in human brain and hiPSC cortical organoids"],"prefix":"10.64898","author":[{"given":"Lei","family":"Cao","sequence":"first","affiliation":[{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yu","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sadaf","family":"Ghorbani","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Yale School of Medicine, New Haven, CT, 06520"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica","family":"Mariani","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Yale School of Medicine, New Haven, CT, 06520"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yanchun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael B.","family":"Fernando","sequence":"additional","affiliation":[{"name":"Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, 10029"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jaroslav","family":"Bendl","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029"},{"name":"Center for Disease Neurogenomics; 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